How does ZFP36 reshape metabolism after growth signals?

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Growth factors induce ZFP36, which binds and decays metabolic enzyme/transporter mRNAs—especially Eno2—tuning glycolytic metabolism.

Source

ZFP36-mediated mRNA decay regulates metabolism

Cicchetto AC, Jacobson EC, Sunshine H, et al. · Cell reports · 2023

doi.org/10.1016/j.celrep.2023.112411 Read the full paper ↗45 citationscc by

Study at a glance

Design: Animal / in-vitro — ZFP36 eCLIP, Eno2 decay, metabolomics, and endothelial Zfp36 loss in retinal angiogenesis
N: MEF and in-vivo angiogenesis assays — no single primary analytic N in stored text
Population: Mouse embryonic fibroblasts and neonatal retinal vasculature models
Outcome: ZFP36-mediated decay of metabolic mRNAs including Eno2

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How does ZFP36 reshape metabolism after growth signals?

These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.

What activates ZFP36 expression and decay activity?

Here, we show that acute growth factor signaling is a potent activator of ZFP36 expression and mRNA decay activity.

Which mRNA classes are bona fide ZFP36 targets?

We quantitatively catalog mRNAs directly bound by ZFP36 and identify metabolic enzymes and nutrient transporters as bona fide targets of ZFP36.

Read passages in the original paper

What they did

Mapped ZFP36 induction and eCLIP targets after growth-factor stimulation in MEFs, validated Eno2 decay, metabolomics, and retinal angiogenesis after endothelial Zfp36 loss.

What they found

ZFP36 family members are acute growth-factor immediate-early genes; they bind many metabolic mRNAs and promote Eno2 mRNA decay; loss elevates ENO2/PEP and alters the metabolome; regulation appears in neonatal retinal angiogenesis.

The limits

What it doesn't show

Does not prove Eno2 is the sole metabolic effector of ZFP36 in every tissue or that ZFP36 drugs would safely remodel metabolism clinically.

Key terms

ZFP36: RNA-binding protein family that promotes ARE-mediated mRNA decay.
ARE: AU-rich element in 3′ UTRs that recruits decay factors.
ENO2: Enolase 2, a glycolytic enzyme producing phosphoenolpyruvate.
eCLIP-seq: Crosslinking method to map RNA-binding protein targets.
Immediate-early gene: Gene induced rapidly by stimuli without needing new protein synthesis cofactors for onset.

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ZFP36 is induced here by:

Common questions

What induces ZFP36 here?

Acute growth-factor / serum signaling.

Key metabolic target validated?

Enolase 2 (Eno2) mRNA decay.

What happens without ZFP36 family?

Metabolic mRNAs/metabolites shift; ENO2 and PEP rise.

In vivo context?

Endothelial ZFP36 regulates ENO2 during retinal angiogenesis.